Thalidomide protects mice against LPS-inducecl shock

A. L. Moreìra, J. Wang, E. N. Sarno, G. Kaplan

Research output: Contribution to journalArticlepeer-review


Thalidomide has been shown to selectively inhibit TNF-α production in vitro by lipopolysaccharide (LPS)-stimulated monocytes. TNF-α has been shown to play a pivotal role in the pathophysiology of endotoxic shock. Using a mouse model of LPS-induced shock, we investigated the effects of thalidomide on the production of TNF-α and other cytokines and on animal survival. After injection of 100-350 μg LPS into mice, cytokines including TNF-α, IL-6, IL-10, IL-1ß, GM-CSF and IFN-γ were measured in the serum. Administration of 200 mg/kg thalidomide to mice before LPS challenge modified the profile of LPS-induced cytokine secretion. Serum TNF-α levels were reduced by 93%, in a dose-dependent manner, and TNF-α mRNA expression in the spleens of mice was reduced by 70%. Serum IL-6 levels were also inhibited by 50%. Thalidomide induced a two-fold increase in serum IL-10 levels. Thalidomide treatment did not interfere with the production of GM-CSF, IL-1ßor IFN-γ. The LD50 of LPS in this model was increased by thalidomide pre-treatment from 150 μg to 300 μg in 72 h. Thus, at otherwise lethal doses of LPS, thalidomide treatment was found to protect animals from death.

Original languageEnglish (US)
Pages (from-to)1199-1207
Number of pages9
JournalBrazilian Journal of Medical and Biological Research
Issue number10
StatePublished - Oct 1997
Externally publishedYes


  • Cytokines
  • Endotoxic shock
  • Inflammation
  • Thalidomide

ASJC Scopus subject areas

  • Biophysics
  • Neuroscience(all)
  • Biochemistry
  • Physiology
  • Immunology
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Cell Biology


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